Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to find out which hemostasis parameters would have the predictive value for the development of preeclampsia, modified antithrombin III (ATM, representative of the antithrombin III-serine esterase complex), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), beta-thromboglobulin (BTG), antithrombin III (AT III), fibrinogen, fibrin(ogen) degradation product (FDP), FDP D-dimer and euglobulin lysis time (ELT) were measured in 20 normal non-pregnant women, 21 normal pregnant women, 6 high-risk pregnant women, 14 preeclampsia pregnant women, and 5 patients with disseminated intravascular coagulation (DIC). Only tPA and AT III were found significantly different between the preeclampsia and the normal or high-risk pregnant women: tPA was found progressively and significantly increased from the normal pregnant, to the high-risk pregnant, then to the preeclampsia women (p less than 0.05). AT III was significantly lower in the preeclampsia than in the normal pregnant (p = 0.0001) or in the high-risk pregnant women (p = 0.002). In the 2nd trimester, tPA, PAI, fibrinogen and FDP were significantly higher, and AT III was significantly lower in the preeclampsia than in the normal pregnant women, whereas in the 3rd trimester, tPA and AT III were significantly higher or lower, respectively, in the preeclampsia than in the normal pregnant women. No significant difference of ATM could be found between the preeclampsia and the normal or high-risk pregnant women. From the present study, we suggest that tPA and AT III would be used as the main predictors, and FDP and D-dimer as the complementary predictors for the development of preeclampsia and should be detected in the normal or high-risk pregnant women.
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PMID:The predictive value of the hemostasis parameters in the development of preeclampsia. 162 Dec 41

Plasma levels of tissue-plasminogen activator.plasminogen activator inhibitor (t-PA.PAI) complex and active PAI were assayed in 58 cases of disseminated intravascular coagulation (DIC). A significant elevation of both parameters was observed in most cases of DIC, especially in patients with non-Hodgkin lymphoma, sepsis, or some patients with acute leukemia, but no such elevation was observed in patients with acute promyelocytic leukemia (APL). The levels of both parameters were higher in cases of DIC with multiple organ failure (MOF) than in those without MOF. Since no elevation of t-PA.PAI complex was observed in most cases of APL, t-PA did not seem to play an important role in the activation of fibrinolytic system in APL. Active PAI, which reflects the inhibitory regulation in fibrinolytic system, was considered to play a role in the progression of MOF. Plasma levels of active PAI were low in the cases of APL, which had no complication of MOF.
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PMID:Changes in plasma levels of tissue-plasminogen activator/inhibitor complex and active plasminogen activator inhibitor in patients with disseminated intravascular coagulation. 130 60

New trends in tests for coagulation and fibrinolysis and advances in diagnosis for the hypercoagulable state and utilization of immunological techniques such as various polyclonal and monoclonal antibodies are reported. We discussed (1) the new markers for hypercoagulable states, (2) differential diagnosis of disseminated intravascular coagulation (DIC) and abnormalities of coagulation in liver cirrhosis (LC), and (3) new markers for fibrinolysis and vascular function. Thrombin-antithrombin III complex (TAT) levels were higher in thrombotic diseases than in healthy controls. Therefore, TAT should be a good marker for hypercoagulation as fibrinopeptide A (FPA) and soluble fibrin monomer complex (SFMC). Measurement of TAT, plasma-alpha 2 plasmin inhibitor complex (PIC), and D dimer were useful for differential diagnosis of DIC and liver cirrhosis. t-PA-PAI complex correlated well with t-PA, but not with fibrinolytic parameters such as PIC. The t-PA-PAI complex may be a good marker for the function of the vascular endothelium.
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PMID:[A new advance in theory of blood coagulation and fibrinolysis and its practical application]. 190 12

We evaluated a new enzyme immunoassay for determination of t-PA-PAI-1 complex (PAI-C) and studied the clinical utility of measuring PAI-C. This assay was performed by the capture/tag antibody technique using polystylene beads, in which the beads were coated with monoclonal antibody against PAI-1 and anti-t-PA polyclonal antibody was tagged (TDC-88, TEIJIN-LIMITED, Japan). The assay gave an excellent sensitivity with a detection limit of 0.1 ng/ml, and we were able to detect a trace amount of PAI-C in normal plasma. PAI-C in 6 volunteers showed significant daytime fluctuations. The normal value of PAI-C in plasma was below 13.8 ng/ml (n = 40). PAI-C levels in patients with accelerated fibrinolysis (n = 31) ranged from 2.9 to 66.4 ng/ml and 15 of them were outside the normal range. However, all of patients with DIC (n = 10) showed abnormally high PAI-C levels. In patients with accelerated fibrinolysis, PAI-C values correlated with t-PA antigen (r = 0.838), PAI-1 antigen (r = 0.519), ATIII activity (r = -0.669) (p less than 0.01) and D dimer levels (r = 0.391, p less than 0.05). However, PAI-C values did not correlate with plasminogen and alpha 2PI activity, alpha 2PI-plasmin complex or the FDP-E level in these patients. Our data suggests that PAI-C may be a new molecular marker that reflects t-PA release from endothelial cells and a useful indicator to study hypercoagulable states.
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PMID:[Evaluation of a new enzyme immunoassay method for determination of t-PA-PAI-1 complex]. 190 14

To evaluate the activation of the extrinsic pathway of coagulation in disseminated intravascular coagulation (DIC), plasma factor VII coagulant activity (FVIIc) and antigen levels (FVIIag) were measured in 81 blood samples obtained from the 56 patients with DIC together with various hemostatic parameters. Plasma FVIIc (77 +/- 40%, range: 11-200%) and FVIIag (76 +/- 43%, range: 16-175%) were significantly lower in DIC subjects than in age-matched controls (FVIIc: 128 +/- 28%, FVII: 128 +/- 31%, p less than 0.01) and correlated significantly with both the antithrombin III and plasminogen activities (p less than 0.001). These results indicated that a decrease in factor VII levels is due to the consumption. However, there were several exceptions which showed elevated factor VII levels. This seems to be due to enhanced liver synthesis of factor VII compensating for the consumption. The level of tPA-PAI-I complex, a marker of pathologic endothelial stimulation, was negatively correlated with FVIIag (r = 0.45, p less than 0.05). Thus, the more the endothelium is pathologically stimulated, the more the extrinsic pathway is activated in DIC. The FVIIc/FVIIag ratio, an index of activation of factor VII zymogen, correlated with FDP and fibrin monomer levels (p less than 0.01). There were no correlations between the thrombin-antithrombin III complex. D-dimer, and alpha 2 antiplasmin-plasmin complex levels and factor VII levels. Considering the underlying diseases. the FVIIc and FVIIag levels were markedly lower in liver cirrhosis, but not significantly different in other diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Plasma factor VII levels in disseminated intravascular coagulation]. 192 Aug 59

There was a markedly significant increase of plasma levels of tissue-type plasminogen activator, plasminogen activator inhibitor 1 (PAI-1) and PAI activity in 3 patients with hemophagocytic histiocytosis (HPH) as compared with DIC patients with multi-organ failure (MOF). Of particular interest was the peculiar increase of PAI-1 levels, that is, the average PAI-1 level was 2,673 ng/ml, while that in DIC patients with MOF was 66 ng/ml. We conclude that the striking increase of plasma PAI-1 levels may be a pathognomonic feature of HPH and may contribute to the pathogenesis of DIC and/or MOF associated with HPH.
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PMID:[Peculiar increase of plasma plasminogen activator inhibitor 1 levels in patients with hemophagocytic histiocytosis]. 231 2

Defibrotide is a polydeoxyribonucleotide-derived anti-ischemic drug with multiple sites of action involving both plasmatic and cellular targets. This agent has been demonstrated to produce profibrinolytic, cytoprotective, and vaso-facilatory actions. Since monocytes are increased in the mediation of some of the pathophysiologic responses seen in ischemic disorders, the functional properties of these cells were investigated in experimental conditions to evaluate their behavior during resting and stimulated states. Defibrotide was supplemented in these systems to determine its modulatory action. In this investigation Defibrotide was found to decrease the PAI-1 levels and may indicate that this may be the mechanism for its profibrinolytic actions. Defibrotide was also found to reduce the procoagulant activity of monocytes in these experimental settings. Both PAI and procoagulant factors play an important role in the pathophysiology of inflammation, DIC, and ischemia. Defibrotide induced reduction of these two factors represents the mechanism whereby this agent produces its therapeutic action.
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PMID:Defibrotide reduces monocyte PAI-2 and procoagulant activity. 766 Jan 47

Plasma levels of tissue-type plasminogen activator antigen (t-PA:Ag), plasminogen activator inhibitor-1 antigen (PAI-1:Ag), the active form of PAI-1 (active PAI) and t-PA.PAI-1 complex (PAI-C) were analyzed in 7 patients with disseminated intravascular coagulation (DIC) syndrome. The levels of t-PA:Ag and PAI-C decreased after amelioration of DIC in 6 patients whose underlying disease improved, but their PAI-1:Ag and active PAI showed various fluctuations. The levels of t-PA:Ag and PAI-C showed a good correlation of r = 0.885. The levels of t-PA:Ag or PAI-C showed an inversed correlation with platelet counts, and correlations with the levels of plasmin.alpha 2PI complex, D dimer and E fragments of FDP. It was considered that plasma levels of PAI-C reflected levels of t-PA released from the endothelial cells, which was related to acceleration of fibrinolysis in DIC patients with improved underlying disease. On the other hand, these levels remained high in a patient whose underlying disease did not improve after recovering from DIC. It was considered that the stimulation of endothelial cells by cancer cells continued to exert an effect.
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PMID:[Fluctuations of tissue-type plasminogen activator.plasminogen activator inhibitor-1 complex in patients with DIC]. 806 36

We found that patients with thrombotic thrombocytopenic purpura (TTP) have significantly elevated plasma thrombin antithrombin III complex (TAT) and FDP-D-dimer levels, while the plasmin-alpha 2 plasmin inhibitor complex (PIC) level was only slightly increased. The tissue-type plasminogen activator (t-PA) level was increased, but it was well correlated with the plasminogen activator inhibitor-I (PAI-I) level. These findings suggest that hypercoagulable and hypofibrinolytic states coexist in these patients, in contrast to patients with disseminated intravascular coagulation, who exhibit coexisting hypercoagulable and hyperfibrinolytic states. Levels of vascular endothelial cell markers, such as PAI-I, thrombomodulin (TM), and t-PA, were increased at the onset of TTP, but the level of von Willebrand factor (vWF) antigen was not increased. The outcome in TTP patients was correlated with plasma t-PA and TM levels but not with TAT or PIC. These results suggest that vascular endothelial cell markers, such as TM and t-PA, are released from injured or stimulated endothelial cells, reflecting the degree of vascular endothelial damage, and that the main factor in the pathogenesis of TTP is vascular endothelial cell injury.
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PMID:Increased levels of vascular endothelial cell markers in thrombotic thrombocytopenic purpura. 826 13

We examined vascular endothelial cell markers, thrombomodulin (TM), plasminogen activator inhibitor-I (PAI-I), tissue plasminogen activator (t-PA), and von Willebrand factor, in 80 patients with disseminated intravascular coagulation (DIC). The levels of thrombin-antithrombin III complex (TAT), plasmin-alpha 2 plasmin inhibitor complex (PIC) and FDP-D-dimer were significantly increased both before and after the onset of DIC, but were not correlated with organ failure or prognosis. However, the PIC/TAT ratio was lower in patients with poor prognosis than in those with good prognosis, and it was also lower in those with organ failure than in those without. Plasma TM, PAI-I, and t-PA levels were increased in DIC patients with organ failure or poor outcome, but were not significantly increased before the onset of DIC. We consider that the prognosis of patients with DIC might be related to organ failure or endothelial cell damage and that plasma levels of TM, PAI-I, and t-PA might be useful in the detection of these disorders and in assessing prognosis. A hypofibrinolytic state might enhance organ failure in patients with DIC.
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PMID:Increased vascular endothelial cell markers in patients with disseminated intravascular coagulation. 826 24


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